Now let’s build on the above facts concerning mutations and natural selection and turn our attention to the idea of creating a whole new gene via evolutionary processes, the first step in creating a new species. This one task is essential if evolution is to have any hope of turning microbes into men. It has supposedly taken six million years for us to evolve from primates to humans, so we will use this time frame as our benchmark time limit. We also differ from primates by 150 million nucleotides. We will ignore this vast difference for the purposes of the exercise. We will assume the new gene only needs 1,000 nucleotides, though the average is closer to 50,000. Is it possible, using only natural processes to construct a single gene of 1,000 nucleotides in six million years? No it is not. Insurmountable problems lie in its developmental path. Here are a few:

1. The Problem of Getting Started

Our first problem is defining the value of the new nucleotide, but we can only assign value to it in relation to superior information, superior function and superior odds of survival that it adds to its existing neighbours and the phenotype. Having random letters begin to fall into an existing text is a slow and tiresome way to create new, superior information. Evolution has no pre-programmed outcome it is heading toward. From the very first piece of new mutational information we have disturbed the existing message and have no pre-existing mandate or message for it to work toward. The concept of a human being did not pre-exist in the mind of natural selection when our primate nucleotide began mutating. Nothing did. There is no such thing as “mother nature”.

To illustrate the point, Richard Dawkins’ famous “Me thinks it is like a weasel” digital evolution experiment only worked because the computer was pre-programmed to look for that exact sentence and favour it each “generation”. Because of this pre-programming, the result was almost miraculous evolution, something natural selection can never do. Natural selection can assign no value to a new mutation unless it is massive in scale, such as a whole linkage block visible at the phenotype level. More on that idea later.

2. The Now Familiar Problem of Near-Neutral Non-Selection

But let’s assume for a moment that we actually have begun to climb Richard Dawkins Mount Improbable and produced the first point mutation containing brand new, more complex information. As we now know, nearly all mutations interfere with the original information contained within the genome, but most of them will only have a tiny negative effect. So most mutations, whether good or bad, fall within Mootoo Kimura’s “effectively neutral mutation” zone. None of these mutations can be selected in or out. They are stuck, and 100,000 harmful mutations are accumulating for every one beneficial mutation. Because of this near-neutral problem we cannot even get to our first selection base in terms of building our new gene. Millions of deleterious mutations would have to embed in the genome before one beneficial mutation appeared that is significant enough to be selected on its own. And as we now know this would take hundreds of thousands of years for each one.

3. The Problem of Securing a Specific Mutation

If we have 300 mutations per individual chimpanzee per generation, this is an exceedingly small percentage of nucleotide disruptions overall, somewhere between one per 3 to 30 million nucleotides per individual, per generation. If we assume 10,000 primates lived within breeding distance of each other and a 10 year breeding cycle, we would have to wait some 3,000 generations for a single pre-determined nucleotide location to mutate. That’s 30,000 years. Once it arrives and overcomes all selection barriers such as near-neutrality, recessiveness, genetic drift, noise, epistasis, and epigenetics it will slowly spread and become fixed in that one location. How many times must the first mutation occur before it has overcome these formidable hurdles? Once fixed, we have to wait for a second and complimentary mutation to turn up right next to it, repeating the exact same cycle, then another and another. The chances of that happening the first try are 30,000 x 3 billion!

4. The Problem of Time

Which leads to the issue of time. Contrary to popular myth, time is not a friend of evolution. Follow the maths: As mentioned previously, at 300 mutations per individual, per generation, a ten year reproductive cycle in primate/primitive humans and a ratio of 100,000 deleterious mutations to every beneficial mutation, it would take an average of  300 generations or about 3,000 years for the very first beneficial mutation to appear, at any random location. Most of the time this lonely beneficial mutation will be then lost or invisible to natural selection due to non-selection, recessiveness, drift, noise, epistasis, linkage blocks, epigenetics and a host of other factors. These complicating factors slow our evolutionary process down significantly and push our time frame out by a factor of 10. This means we wait another 30,000 years for the next mutation. But the second mutation could be anywhere, no one determines where in the 3 billion nucleotide genome they will occur. There is a 3 billion to one chance it will be next to the first mutation. Even if there were only 3 million nucleotides in the genome, one thousanthmofmwhat there really was, it would still take 90 billion years to guarantee one would appear next to the original.

We are now looking at the impossibility of creating just our first two mutations, regardless of our infamous non-selection box for all but the most severe mutations. However, just say that by luck we do get two consecutive mutations because they are in a mutational hotspot. This new information will not make sense unless it becomes much more significant in the same way that this sentence doesn’t make sense when two random letters of one word are changed.

When not pre-programmed to look for the sentence, Richard Dawkins’ weasel experiment took 10⁴⁰ (forty duodecillion!) attempts before his computer completed the weasel sentence. Just add 29 more zeros to the 90 billion years mentioned above! So, if it is impossible to produce that simple sentence via random changes, how much more a gene that is the equivalent of several pages of text? We are now looking at an infinite number of years to stabilise our first simple 1,000 nucleotide gene. The rarity of beneficial mutations is a great millstone around the neck of evolutionary theory. Contrary to popular myth, chimps tapping on keyboards will never produce Shakespeare, regardless of time.

Then, just to add insult to injury, in the meantime most of those 300 deleterious mutations per generation are invisible to selection and have multiplied to 900,000 mistakes in just those first 3,000 generations. That’s 180,000,000 in six million years or 16% of the genome. This is enough to wipe out a species.

5. The Problem of Drift

For arguments sake let’s assume our first functional nucleotide “sentence” is now fixed in our first individual primate. It must then spread to the whole population. Natural selection must now actively select individuals with this mutational message otherwise genetic drift and noise will condemn it to extinction. What if the “sentence” is recessive, what if that individual was killed by a lion? Noise now kicks in and slows down the spread of this new information. We are back to square one in an instant and the exact same set of mutations would have to occur all over again.

John Haldane researched this problem in 1957 and came up with the generous figure of one nucleotide fixed every 6,000 years at best in humans as a speed limit for evolutionary advance. Taking his figures on face value we are already far outside a legitimate time frame for evolution to work its magic of transforming 150 million nucleotides from that of primate to humans. This problem is now known as “Haldane’s Dilemma” and is still unresolved today. This makes our total of 6 million years for our one single 1,000 nucleotide gene look exceedingly generous indeed!

But Haldane’s figure is a furphy. Haldane assumed mutations don’t have to appear next to each other, which we know they do. He wrongly assumed individual nucleotides could all be selected (no near-neutrals) and selected independently (no epistasis or linkage blocks). We now know both of these assumptions are false. Recalculating the same Haldane Dilemma using realistic parameters ends with an abject impossibility. Mount Improbable is beginning to look like an overhanging cliff face.

6. The Problem of Linkage Blocks

Now, about those darn genetic linkage blocks. Since we now know that that they are passed on to offspring in their entirety, they are passing on 100,000 near-neutral, minor and major deleterious mutations for every one lonely beneficial mutation. This creates two problems.

First, as previously mentioned, it is a form of Muller’s Ratchet, even though we are talking about sexual recombination every generation. (Sexual recombination was Muller’s argument for why his ratchet did not apply to humans and evolution could proceed.) Linkage blocks turn sexual reproduction into a form of asexual reproduction. This was borne out in a study by S.B. Gabriel in 2002 that found that there is “little evidence for the recombination” of haploptypes (linkage blocks) since the origin of modern man!

Second, there is simply no way a single beneficial mutation will be visible to selection when out-numbered so dramatically by deleterious mutations. These two indisputable facts are irreconcilable with the concept of monkeys to man evolution.

To understand the profound importance of linkage blocks in genetics, consider the opposite problem, linkage blocks not being passed on in their entirety. This creates a major problem for the survival of that individual. For example those who suffer from Turner Syndrome are missing one of the two female X chromosomes. So the heritability of entire genetic linkage blocks is crucial for survival. A 2003 study Sarah Tishkoff and Brian Verrelli confirmed this fact. Genes, and their slightly smaller cousins, linkage blocks, are simply too important for survival to be selected out or replaced as a whole. This creates a new level of certainty that all DNA must degenerate over time, not evolve. This is another reason why evolutionary geneticists assume individual selection of nucleotides. Their models do not work when faced with the reality of large scale genetic linkage blocks.

To illustrate the futility of the situation, imagine for a moment that we have indeed suddenly achieved 100 beneficial mutations in a single area of primate DNA. While waiting for the next beneficial mutation to come along, the entire linkage block, including our newly-minted 100 beneficial mutations, will begin to degenerate as the dreaded 100,000:1 mutational ratio kicks in. One step forward, a hundred thousand backwards.

7. The Problem of Fitness Valleys

Now let’s be generous and assume we have achieved 500 beneficial mutations, our new super-simple gene is semi-complete and almost fixed in the whole population. Natural selection has reached the point where it is blindly experimenting with heritable, visible new half completed forms, but with no goal in sight. We now enter what is called a “fitness valley”. During this experimental phase we have to expect a period of time when the genetic fitness of an individual or a species is severely compromised. They enter the dreaded fitness valley. Contrary to modern myth, a half-completed gene is neither neutral nor beneficial, it is deleterious. Natural selection is therefore more likely to eliminate these individuals. If a fitness valley is brief it might be crossed but deep and frequent fitness valleys are likely to be a lethal death-spiral for a species. Since evolutionary theory constantly requires the endless crossing of these deep fitness valleys, natural selection now becomes its enemy, not friend.

8. The Problem of Irreducible Complexity

As just mentioned, none of the component features of the new mutational function have any meaning when half finished. Only when they come together and are complete will they perform a new and superior function. In addition to this, all component parts must come together simultaneously in a perfect synthesis. The more we learn about natural systems the more complex they become. We now know that as the number of component parts increases linearly, the number of interactions increases exponentially. Thus there is an irreducible complexity to all living systems.

This concept of irreducible complexity has been savagely attacked by evolutionary biologists. They point to the evolution of the eye from a “simple” light sensitive spot as the first step toward a modern eye. How complex is a “simple” light spot? To answer this question, consider a small sample section of the chemical complexity you are using right now to read this essay:

“When light first strikes the retina a photon interacts with a molecule called 11-cis-retinal, which rearranges within picoseconds to trans-retinal. (a picosecond is 10^-12 seconds, about the time it takes light to travel the breadth of a single human hair.) The change in the shape of the retinal molecule forces a change in the shape of the protein, rhodopsin, to which the retinal is tightly bound. The protein’s metamorphosis alters its behaviour. Now called metarhodopsin II, the protein sticks to another protein, called transducin. Before bumping into metarhodopsin II, transducin had tightly bound a small molecule called GDP. But when transducin interacts with metarhodopsin II, the GDP falls off, and a molecule called GTP binds to transducin. GTP is closely related to, but different from, GDP. GTP-transducin-metarhodopsin II now binds to a protein called phosphodiesterase, located in the inner membrane of the cell. When attached to metarhodopsin II and its entourage, the phosphodiesterase acquires the chemical ability to ‘cut’ a molecule called cGMP, a chemical relative of both GDP and GTP. Initially there are a lot of cGMP molecules in the cell, but the phosphodiesterase lowers its concentration, just as a pulled plug lowers the water level in a bathtub.”

Phew!

If you take a single component out of this process and the system collapses, sight is compromised. Mutations can never create this level of complex information. But even if they could create some complex information, they could not create enough of it. If they create enough, there is just not enough time to complete the job, even in evolutionary deep time. Even if there was enough time, selection would eliminate inferior function. The eye never evolved.

In addition, for every level of complexity in any biological function you can think of, there is 10 to 100 times more complexity in the genetic instructions behind them. Any evolutionary explanation of biological functionality, such as the eye, must also give a credible evolutionary explanation for the irreducible complexity in the genetic instructions behind it. But it can’t because both had to come into existence at the same time. Neither can exist without the other. And we haven’t even started talking about the almost infinite issue of irreducible cellular complexity!

9. The Problem of Selection Cost

Now let’s suppose we actually did manage to somehow overcome all the obstacles listed in this entire essay and created a new gene, and that natural selection actually works. Do we have enough excess primitive humanoids every generation to fund this natural selection process? Before we can eliminate those carrying significant genetic defects, we have to also account for those who will die unnatural deaths, early deaths, do not reproduce etc. Have primates evolving into humans reproduced at such a level though the last 6 million years to afford enough natural selection to eliminate the vast majority of the 100,000:1 ratio of deleterious mutations on top of all environmental costs? The short answer is no, and large numbers of human geneticists, such as Campbell & Eichler, Charlesworth, Haldane, Higgins, Loewe, Lynch, Muller, Nachman, Parsons, Rands, ReMine and now John Sanford are concerned about it.

10. The Problem of Extinction

Now suppose we jumped every rock and boulder on our way up Mount Improbable and did indeed begin the process of large scale progression from primate to human. The next problem we face is that of the rapid genetic degeneration of the newly acquired features. We now know that the mutation rate is between 100 and 1,000 per individual per generation. We also know that primates and humans differ by 150 million nucleotides. Extrapolating from these figures we find that, generously assuming the upper limit of 1,000 mutations per breeding cycle and 10 years between cycles, there has only been enough time for approximately 800 beneficial mutations to appear, even after 6 million years. And that’s at any random location in the genome. (This figure ignores all barriers to fixing these mutations discussed above.) In the meantime after close to 1 million generations, we would all now be living with around 180 million deleterious mutations that accumulated during the same period of time. If still alive we be far inferior to our ancestors, dreadfully deformed and diseased.

Conclusion

In conclusion to this section, there are so many boulders, cliff faces, obstacles and ravines on Mount Improbable that is clearly Mount Impossible. As you can now see, evolution cannot even create a simple gene of 1,000 nucleotides in the time we are supposed to have evolved from chimpanzees, let alone a whole set of more sophisticated genes and the 150 million nucleotides that differentiate us from chimps. Recent sequencing of human and chimpanzee Y chromosomes further destroys these evolutionary assumptions.

Evolutionists have cleverly confused the meaning of evolution in the minds of the public. They have treated adaptation to an environment via informational-loss, and its opposite, informational-gain into higher life forms, as if they were the same thing. Evolutionary ideas are like Communist dogma; eloquent in theory and all-encompassing, but not reflecting reality.

Mutations cannot create increasing genetic complexity and natural selection is a one-way street of information elimination. So we did not evolve from chimpanzees.

Evolution does not exist in the real world, but something else does…

Part Five of this essay will now look at the plentiful evidence for genetic entropy in the real world.